The Relationship among Chronic Pain, Opiates, and Sleep

Abstract

Thesis (Ph.D.)--University of Rochester. School of Nursing. Dept. of Nursing, 2008.The overall aim of this study was to examine the relationships among chronic pain, opiates, respiration, and sleep in a sample of subjects referred for assessment of sleep disorders. This study assessed: (a) whether increasing dosages of opiate predict severity of sleep disordered breathing, sleep architecture, sleep continuity abnormalities, and/or excessive daytime sleepiness; (b) whether the study groups ([no pain vs. pain] and [pain minus opiate treatment vs. pain plus opiate treatment]) differed with respect to severity of sleep disordered breathing, sleep architecture, sleep continuity abnormalities; (c) whether the known risk factors for sleep disordered breathing differed for persons with and without chronic pain, and (d) whether intensity of pain predicted severity of sleep disordered breathing. Methods A descriptive cross sectional study was conducted. There were two types of independent variables, (a) risk factors for sleep disordered breathing (BMI, age, gender, number of systems affected by co-morbid diseases, and presence of anatomical abnormalities typical of obstructive sleep apnea), and (b) those that were directly related to the investigational hypothesis (pain incidence and intensity and/or opiate use and dose). Dependent Variables included: measures of sleep disordered breathing (e.g., frequency of central and obstructive events), sleep architecture (e.g., percent of stages 1-4 and REM), and sleep continuity measures (e.g., Sleep Latency, Number of Awakenings, and Total Sleep Time). After orthogonally coding for group membership, regression models were used for statistical analysis. Pain, Opiates and Sleep Results Data was collected on a total of 419 subjects (no pain [n = 171], pain –opiate Tx [n = 187], and pain +opiate Tx [n = 61]). Sample demographic (mean +/- SD) was as follows: age 50 yr + 12.; 51% male; BMI 33.8 + 7; Epworth Sleepiness Scale 10.3 + 5; pain intensity 3.8 + 2 (0-10 scale); morphine equivalent dose 152 + 195 mg; and 98% of subjects with pain had non-malignant chronic pain. Per study hypotheses (a) there was a positive dose response relationship between amount of opiate and frequency of central apneic events and percent of stage 3/4 sleep; (b) the [no pain vs. pain] group comparison revealed that subjects with pain had a lower percent of stage 1 sleep, and the [pain minus opiate vs. pain plus opiate]) group comparison revealed that subjects treated with opiates had significantly more central apneic events, more stage 2 sleep and less REM sleep; (c) the known risk factors for sleep disordered breathing differ in persons with and without chronic pain (chronic pain subjects were older, female and suffered from more comorbidity); (d) there was a relationship between pain intensity and frequency of central apneic events and obstructive apneic events. Greater pain intensity was associated with more frequent central apneic events and fewer obstructive apneic events. Conclusion These data suggest that the management of chronic pain with opiates is not likely to exacerbate obstructive sleep apnea at stable opiate doses; however; central sleep apnea may be worsened. The magnitude of the effect is modest, and the clinical relevance of the effect is unknown. Thus, the potential for marginal respiratory disturbance (an increase of 2.8 central events for every 100 mg. morphine equivalent opiate dose) must be weighed against the therapeutic value of pain management with opiates